A recent paper examined if use of the antibiotic cotrimoxazole was correlated with resistance in three different bacterial pathogens, Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. To quickly summarize, in one species, S. pneumoniae, resistance was correlated with use, whereas it was not for the other two species. While the study is fine for what it is, it inadvertently highlights a problem most surveillance systems have:

they don’t incorporate genetic information.

Without genotypic information, we don’t really know what happened. Is the correlation spurious, in that a strain which happens to be resistant, spread rapidly, or is this a selective response to antibiotic use? Previous studies (discussed here) have shown that change in antibiotic resistance is often not correlated with antibiotic use. Instead, changes in the frequency of resistance are due to the turnover in (replacement of) clones that appear to have little to do with antibiotic resistance (believe it or not, bacteria actually do things other than resist antibiotics…).

Note that I refer to clones–a group of closely related strains*. It’s hard, if not impossible, to determine a clone without genetic information. Unfortunately, most surveillance systems don’t collect genetic information, and, if they do, it’s usually from a non-random subset (very small subset) of strains (there are exceptions; virtually all of these exceptional surveillance systems are federally funded).

Now, if there were only a microbiologist with access to a big ol’ genome center who gave a damn about this….

*If this sounds vague, it is. Obviously, the resolution of the method, along with decisions by researchers, will determine which isolates belong to a clone.